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Increased expression of senescence markers in cystic fibrosis airways

Overview of attention for article published in American Journal of Physiology: Lung Cellular & Molecular Physiology, March 2013
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Title
Increased expression of senescence markers in cystic fibrosis airways
Published in
American Journal of Physiology: Lung Cellular & Molecular Physiology, March 2013
DOI 10.1152/ajplung.00091.2012
Pubmed ID
Authors

Bernard M. Fischer, Jessica K. Wong, Simone Degan, Apparao B. Kummarapurugu, Shuo Zheng, Prashamsha Haridass, Judith A. Voynow

Abstract

Cystic Fibrosis (CF) is a chronic lung disease characterized by chronic neutrophilic airway inflammation and increased levels of neutrophil elastase (NE) in the airways. We have previously reported that NE treatment triggers cell cycle arrest. Cell cycle arrest can lead to senescence, a complete loss of replicative capacity. Importantly, senescent cells can be proinflammatory and would perpetuate CF chronic inflammation. By immunohistochemistry, we evaluated whether airway sections from CF and control subjects expressed markers of senescence, including p16(INK4a) (p16), a cyclin-dependent kinase inhibitor, phospho-Histone H2A.X (γH2A.X), and phospho-checkpoint 2 kinase (phospho-Chk2), which are also DNA damage response markers. Compared with airway epithelium from control subjects, CF airway epithelium had increased levels of expression of all three senescence markers. We hypothesized that the high load of NE in the CF airway triggers epithelial senescence by upregulating expression of p16, which inhibits cyclin-dependent kinase 4 (CDK4). Normal human bronchial epithelial (NHBE) cells, cultured in air-liquid interface were treated with NE (0, 200, and 500 nM) to induce visible injury. Total cell lysates were collected and evaluated by Western analysis for p16 protein expression and CDK4 kinase activity. NE significantly increased p16 expression and decreased CDK4 kinase activity in NHBE cells. These results support the concept that NE triggers expression of senescence markers in CF airway epithelial cells.

Twitter Demographics

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Mendeley readers

The data shown below were compiled from readership statistics for 42 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Australia 1 2%
Unknown 41 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 11 26%
Researcher 9 21%
Student > Master 4 10%
Other 3 7%
Student > Doctoral Student 3 7%
Other 7 17%
Unknown 5 12%
Readers by discipline Count As %
Agricultural and Biological Sciences 11 26%
Medicine and Dentistry 9 21%
Biochemistry, Genetics and Molecular Biology 8 19%
Pharmacology, Toxicology and Pharmaceutical Science 2 5%
Chemistry 2 5%
Other 2 5%
Unknown 8 19%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 07 May 2013.
All research outputs
#3,921,328
of 4,681,163 outputs
Outputs from American Journal of Physiology: Lung Cellular & Molecular Physiology
#502
of 640 outputs
Outputs of similar age
#74,483
of 90,166 outputs
Outputs of similar age from American Journal of Physiology: Lung Cellular & Molecular Physiology
#6
of 7 outputs
Altmetric has tracked 4,681,163 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 640 research outputs from this source. They receive a mean Attention Score of 2.7. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 7 others from the same source and published within six weeks on either side of this one.